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Newcastle disease virus (NDV) strain R2B, with an altered fusion protein cleavage site, was used as a viral vector to deliver the immunogenic genes VP2 and VP1 of chicken infectious anaemia virus (CIAV) to generate a bivalent vaccine candidate against these diseases in chickens. The immunogenic genes of CIAV were expressed as a single transcriptional unit from the NDV backbone and the two CIA viral proteins were obtained as separate entities using a self-cleaving foot-and-mouth disease virus 2A protease sequence between them. The recombinant virus (rR2B-FPCS-CAV) had similar growth kinetics as that of the parent recombinant virus (rR2B-FPCS) in vitro with similar pathogenicity characteristics. The bivalent vaccine candidate when given in specific pathogen-free chickens as primary and booster doses was able to elicit robust humoral and cell-mediated immune (CMI) responses obtained in a vaccination study that was conducted over a period of 15 weeks. In an NDV and CIAV ELISA trial, there was a significant difference in the titres of antibody between vaccinated and control groups which showed slight reduction in antibody titre by 56 days of age. Hence, a second booster was administered and the antibody titres were maintained until 84 days of age. Similar trends were noticed in CMI response carried out by lymphocyte transformation test, CD4+ and CD8+ response by flow cytometry analysis and response of real time PCR analysis of cytokine genes. Birds were challenged with virulent NDV and CIAV at 84 days and there was significant reduction in the NDV shed on the 2nd and 4th days post challenge in vaccinated birds as compared to unvaccinated controls. Haematological parameters comprising PCV, TLC, PLC and PHC were estimated in birds that were challenged with CIAV that indicated a significant reduction in the blood parameters of controls. Our findings support the development and assessment of a bivalent vaccine candidate against NDV and CIAV in chickens.

The present study explored the immunological correlates of protection mediated by a live bivalent vaccine consisting of herpesvirus of turkeys (HVT) and SB-1 against infection with the RB1B strain of Marek's disease virus (MDV). Compared to unvaccinated infected chickens, vaccinated protected birds had lower expression of interleukin (IL)-6, IL-10 and IL-18 genes in spleen. However, there was no difference between these two groups of birds in the expression of interferon (IFN)-γ, IL-4, IL-12 and inducible nitric oxide synthase (iNOS) genes on day 21 post-infection. Furthermore, protection was associated with lower MDV genome load in spleen but not in feather tips, suggesting that vaccination had little or no effect on curtailing virus transmission. In conclusion, vaccination with a bivalent MD vaccine was associated with distinct cytokine expression patterns in spleen and modulation of cytokine responses by the vaccine may play a role in mediation of protection.

Probiotics reduce stress-related inflammation and abnormal behaviors in humans and rodents via regulation of the microbiota-gut-brain axis. The objective of this study was to determine if probiotic, Bacillus subtilis, has similar functions in broiler chickens under heat stress (HS). Two hundred forty 1-d-old broiler chicks were assigned to 48 pens with 4 treatments: Thermoneutral (TN)-RD (regular diet), TN-PD (the regular diet mixed with 1 × 106 CFU/g feed probiotic), HS-RD and HS-PD. Probiotic (Sporulin) was fed from day 1; and HS at 32°C for 10 h daily was initiated at day 15. The data showed that final BW, average daily gain , and feed conversion efficiency were improved in PD groups as compared to RD groups regardless of the ambient temperature (P < 0.01). Heterophil to lymphocyte ratio was affected by treatment and its value was in the order of HS-RD > HS-PD > TN-RD > TN-PD birds (P < 0.01). Compared to TN birds, HS birds spent more time in wing spreading, panting, squatting close to the ground, drinking, sleeping, dozing, and sitting but spent less time in eating, standing, and walking (P < 0.05 or 0.01). In addition, HS birds had greater levels of hepatic IL-6, IL-10, heat shock protein (HSP)70, and HSP70 mRNA expression (P < 0.01) and greater levels of cecal IgA and IgY (P < 0.01) compared to TN birds. Within TN groups, TN-PD birds had greater concentrations of hepatic IL-10 (P < 0.05) and cecal IgA (P < 0.01) than TN-RD birds. Within HS groups, HS-PD birds spent less time in wing spreading, panting, squatting close to the ground, drinking, sleeping, dozing, and sitting but spent more time in eating, foraging, standing, and walking than HS-RD birds (P < 0.05 or 0.01). The HS-PD birds also had lower concentrations of hepatic IL-6 and HSP70 (P < 0.01), whereas greater levels of IL-10 (P < 0.05) and lower concentrations of cecal IgA and IgY (P < 0.01). These results indicate that broilers fed the probiotic, B. subtilis, are able to cope with HS more effectively by ameliorating heat-induced behavioral and inflammatory reactions through regulation of microbiota-modulated immunity.

The massive meat production of broiler chickens make them continuously exposed to potential stressors that stimulate releasing of stress-related hormones like corticosterone (CORT) which is responsible for specific pathways in biological mechanisms and physiological activities. Therefore, this research was conducted to evaluate a wide range of responses related to broiler performance, immune function, plasma biochemistry, related gene expressions and cell death morphology during and after a 7-day course of CORT injection. A total number of 200 one-day-old commercial Cobb broiler chicks were used in this study. From 21 to 28 d of age, broilers were randomly assigned to one of 2 groups with 5 replicates of 20 birds each; the first group received a daily intramuscular injection of 5 mg/kg BW corticosterone dissolved in 0.5 ml ethanol:saline solution (CORT group), while the second group received a daily intramuscular injection of 0.5 ml ethanol:saline only (CONT group). Growth performance, including body weight (BW), daily weight gain (DG), feed intake (FI) and feed conversion ratio (FC), were calculated at 0, 3 and 7 d after the start of the CORT injections. At the same times, blood samples were collected in each group for hematological (TWBC's and H/L ratio), T- and B-lymphocytes proliferation and plasma biochemical assays (total protein, TP; free triiodothyronine hormone, fT3; aspartate amino transaminase, AST; and alanine amino transaminase, ALT). The liver, thymus, bursa of Fabricius and spleen were dissected and weighed, and the mRNA expression of insulin-like growth factor 1 gene (IGF-1) in liver and cell-death-program gene (caspase-9) in bursa were analyzed for each group and time; while the apoptotic/necrotic cells were morphologically detected in the spleen. From 28 to 35 d of age, broilers were kept for recovery period without CORT injection and the same sampling and parameters were repeated at the end (at 14 d after initiation of the CORT injection). In general, all parameters of broiler performance were negatively affected by the CORT injection. In addition, CORT treatment decreased the plasma concentration of fT3 and the mRNA expression of hepatic IGF-1. A significant increase in liver weight accompanied by an increase in plasma TP, AST and ALT was observed with CORT treatment, indicating an incidence of liver malfunction by CORT. Moreover, the relative weights of thymus, bursa and spleen decreased by the CORT treatment with low counts of TWBC's and low stimulation of T & B cells while the H/L ratio increased; indicating immunosuppressive effect for CORT treatment. Furthermore, high expression of caspase-9 gene occurred in the bursa of CORT-treated chickens, however, it was associated with a high necrotic vs. low apoptotic cell death pathway in the spleen. Seven days after termination of the CORT treatment in broilers, most of these aspects remained negatively affected by CORT and did not recover to its normal status. The current study provides a comprehensive view of different physiological modulations in broiler chickens by CORT treatment and may set the potential means to mount a successful defense against stress in broilers and other animals as well.

Campylobacter jejuni is the leading cause of bacterial food-borne infection; chicken meat is its main source. C. jejuni is considered commensal in chickens based on experimental models unrepresentative of commercial production. Here we show that the paradigm of Campylobacter commensalism in the chicken is flawed. Through experimental infection of four commercial breeds of broiler chickens, we show that breed has a significant effect on C. jejuni infection and the immune response of the animals, although these factors have limited impact on the number of bacteria in chicken ceca. All breeds mounted an innate immune response. In some breeds, this response declined when interleukin-10 was expressed, consistent with regulation of the intestinal inflammatory response, and these birds remained healthy. In another breed, there was a prolonged inflammatory response, evidence of damage to gut mucosa, and diarrhea. We show that bird type has a major impact on infection biology of C. jejuni . In some breeds, infection leads to disease, and the bacterium cannot be considered a harmless commensal. These findings have implications for the welfare of chickens in commercial production where C. jejuni infection is a persistent problem. IMPORTANCE Campylobacter jejuni is the most common cause of food-borne bacterial diarrheal disease in the developed world. Chicken is the most common source of infection. C. jejuni infection of chickens had previously not been considered to cause disease, and it was thought that C. jejuni was part of the normal microbiota of birds. In this work, we show that modern rapidly growing chicken breeds used in intensive production systems have a strong inflammatory response to C. jejuni infection that can lead to diarrhea, which, in turn, leads to damage to the feet and legs on the birds due to standing on wet litter. The response and level of disease varied between breeds and is related to regulation of the inflammatory immune response. These findings challenge the paradigm that C. jejuni is a harmless commensal of chickens and that C. jejuni infection may have substantial impact on animal health and welfare in intensive poultry production . Campylobacter jejuni is the most common cause of food-borne bacterial diarrheal disease in the developed world. Chicken is the most common source of infection. C. jejuni infection of chickens had previously not been considered to cause disease, and it was thought that C. jejuni was part of the normal microbiota of birds. In this work, we show that modern rapidly growing chicken breeds used in intensive production systems have a strong inflammatory response to C. jejuni infection that can lead to diarrhea, which, in turn, leads to damage to the feet and legs on the birds due to standing on wet litter. The response and level of disease varied between breeds and is related to regulation of the inflammatory immune response. These findings challenge the paradigm that C. jejuni is a harmless commensal of chickens and that C. jejuni infection may have substantial impact on animal health and welfare in intensive poultry production .

Zoonotic influenza A viruses of avian origin can cause severe disease in individuals, or even global pandemics, and thus pose a threat to human populations. Waterfowl and shorebirds are believed to be the reservoir for all influenza A viruses, but this has recently been challenged by the identification of novel influenza A viruses in bats 1 , 2 . The major bat influenza A virus envelope glycoprotein, haemagglutinin, does not bind the canonical influenza A virus receptor, sialic acid or any other glycan 1 , 3 , 4 , despite its high sequence and structural homology with conventional haemagglutinins. This functionally uncharacterized plasticity of the bat influenza A virus haemagglutinin means the tropism and zoonotic potential of these viruses has not been fully determined. Here we show, using transcriptomic profiling of susceptible versus non-susceptible cells in combination with genome-wide CRISPR–Cas9 screening, that the major histocompatibility complex class II (MHC-II) human leukocyte antigen DR isotype (HLA-DR) is an essential entry determinant for bat influenza A viruses. Genetic ablation of the HLA-DR α-chain rendered cells resistant to infection by bat influenza A virus, whereas ectopic expression of the HLA-DR complex in non-susceptible cells conferred susceptibility. Expression of MHC-II from different bat species, pigs, mice or chickens also conferred susceptibility to infection. Notably, the infection of mice with bat influenza A virus resulted in robust virus replication in the upper respiratory tract, whereas mice deficient for MHC-II were resistant. Collectively, our data identify MHC-II as a crucial entry mediator for bat influenza A viruses in multiple species, which permits a broad vertebrate tropism. The DR isotype of the human leukocyte antigen of the MHC class II—or its homologues in bats, pigs, mice and chickens—is an essential cell entry determinant for bat influenza A viruses.

Marek’s disease (MD), caused by Marek’s disease virus (MDV), is a commercially important neoplastic disease of poultry which is only controlled by mass vaccination. Importantly, vaccines that can provide sterile immunity and inhibit virus transmission are lacking; such that vaccines are only capable of preventing neuropathy, oncogenic disease and immunosuppression, but are unable to prevent MDV transmission or infection, leading to emergence of increasingly virulent pathotypes. Hence, to address these issues, developing more efficacious vaccines that induce sterile immunity have become one of the important research goals for avian immunologists today. MDV shares very close genomic functional and structural characteristics to most mammalian herpes viruses such as herpes simplex virus (HSV). MD also provides an excellent T cell lymphoma model for gaining insights into other herpesvirus-induced oncogenesis in mammals and birds. For these reasons, we need to develop an in-depth knowledge and understanding of the host-viral interaction and host immunity against MD. Similarly, the underlying genetic variation within different chicken lines has a major impact on the outcome of infection. In this review article, we aim to investigate the pathogenesis of MDV infection, host immunity to MD and discuss areas of research that need to be further explored.

A Newcastle disease virus (NDV)-vectored vaccine expressing clade 2.3.4.4b H5 Hemagglutinin was developed and assessed for efficacy against H5N1 highly pathogenic avian influenza (HPAI) in specific pathogen-free (SPF) chickens, broilers, and domestic ducks. In SPF chickens, the live recombinant NDV-vectored vaccine, rK148/22-H5, achieved complete survival against HPAI and NDV challenges and significantly reduced viral shedding. Notably, the live rK148/22-H5 vaccine conferred good clinical protection in broilers despite the presence of maternally derived antibodies. Good clinical protection was observed in domestic ducks, with decreased viral shedding. It demonstrated complete survival and reduced cloacal viral shedding when used as an inactivated vaccine from SPF chickens. The rK148/22-H5 vaccine is potentially a viable and supportive option for biosecurity measure, effectively protecting in chickens against the deadly clade 2.3.4.4b H5 HPAI and NDV infections. Furthermore, it aligns with the strategy of Differentiating Infected from Vaccinated Animals (DIVA).

Goose astrovirus (GAstV) is a major threat to the goose industry, with no effective drugs or vaccines available. Developing safe and effective prevention and treatment strategies is essential to reduce its impact. In our study, we used the GAstV GDCS strain as the vaccine antigen and found that a 1 ‰ formaldehyde concentration effectively inactivated the virus after 24 h at 37 °C. The inactivated virus antigen was subsequently emulsified with white oil to formulate the GAstV inactivated vaccine. This vaccine was administered four times to 22-week-old laying hens, and IgY was subsequently purified from the egg yolk using the polyethylene glycol (PEG) precipitation method. After the fourth immunization, IgY concentration was 3.133 mg/mL. SDS-PAGE showed IgY has a 65 kDa heavy chain and a 25 kDa light chain. The IgY effectively neutralized GAstV in vitro with a titer of up to 2^9.67. Administering IgY to goslings effectively prevents and treats GAstV infection by reducing symptoms, mortality, tissue damage, and viral load. These findings offer significant tools for the clinical prevention and management of GAstV infection.

Poultry infected with Salmonella mount an immune response initially, however the immune responses eventually disappear leading the bird to be a carrier of Salmonella . The hypothesis of this study is that Salmonella infection induces T regulatory cell numbers and cytokine production and suppress host T cells locally in the gut to escape the host immune responses. An experiment was conducted to comparatively analyze the effect of S . enterica ser. Enteritidis ( S . Enteritidis) and S . enterica ser. Heidelberg ( S . Heidelberg) infection on CD4 + CD25 + T regulatory cell properties in chickens. A total of 144 broiler chicks were randomly distributed into three experimental groups of non-infected control, S . Enteritidis infected and S . Heidelberg infected groups. Chickens were orally inoculated with PBS (control) or 5x10 6 CFU/mL of either S . Enteritidis or S. Heidelberg at 3 d of age. Each group was replicated in six pens with eight chickens per pen. Chickens infected with S . Enteritidis had 6.2, 5.4, and 3.8 log 10 CFU/g, and chickens infected with S . Heidelberg had 7.1, 4.8, and 4.1 log 10 CFU/g Salmonella in the cecal contents at 4, 11, and 32 dpi, respectively. Both S . Enteritidis and S . Heidelberg were recovered from the liver and spleen 4 dpi. At 4, 11, and 32 dpi, chickens infected with S . Enteritidis and S . Heidelberg had increased CD4 + CD25 + cell numbers as well as IL-10 mRNA transcription of CD4 + CD25 + cells compared to that in the control group. CD4 + CD25 + cells from S . Enteritidis- and S . Heidelberg-infected chickens and restimulated with 1 μg antigen in vitro , had higher (P < 0.05) IL-10 mRNA transcription than the CD4 + CD25 + cells from the non-infected controls Though at 4dpi, chickens infected with S . Enteritidis and S . Heidelberg had a significant (P < 0.05) increase in CD4 + CD25 - IL-2, IL-1β, and IFNγ mRNA transcription, the CD4 + CD25 - IL-2, IL-1β, and IFNγ mRNA transcription, were comparable to that in the control group at 11 and 32dpi identifying that the host inflammatory response against Salmonella disappears at 11 dpi. It can be concluded that S . Enteritidis and S . Heidelberg infection at 3 d of age induces a persistent infection through inducing CD4 + CD25 + cells and altering the IL-10 mRNA transcription of CD4 + CD25 + cell numbers and cytokine production in chickens between 3 to 32 dpi allowing chickens to become asymptomatic carriers of Salmonella after 18 dpi.